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Toxins 2014, 6(5), 1505-1511;

Uremic Toxins and Lipases in Haemodialysis: A Process of Repeated Metabolic Starvation

Department of Public Health and Clinical Medicine, University of Umeå, Umeå SE-901 87, Sweden
Received: 11 March 2014 / Revised: 11 April 2014 / Accepted: 14 April 2014 / Published: 30 April 2014
(This article belongs to the Special Issue Uremic Toxins)
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Severe kidney disease results in retention of uremic toxins that inhibit key enzymes for lipid breakdown such as lipoprotein lipase (LPL) and hepatic lipase (HL). For patients in haemodialysis (HD) and peritoneal dialysis (PD) the LPL activity is only about half of that of age and gender matched controls. Angiopoietin, like protein 3 and 4, accumulate in the uremic patients. These factors, therefore, can be considered as uremic toxins. In animal experiments it has been shown that these factors inhibit the LPL activity. To avoid clotting of the dialysis circuit during HD, anticoagulation such as heparin or low molecular weight heparin are added to the patient. Such administration will cause a prompt release of the LPL and HL from its binding sites at the endothelial surface. The liver rapidly degrades the release plasma compound of LPL and HL. This results in a lack of enzyme to degrade triglycerides during the later part of the HD and for another 3–4 h. PD patients have a similar baseline level of lipases but are not exposed to the negative effect of anticoagulation. View Full-Text
Keywords: hepatic lipase; lipoprotein lipase; haemodialysis; peritoneal dialysis; malnutrition hepatic lipase; lipoprotein lipase; haemodialysis; peritoneal dialysis; malnutrition

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Stegmayr, B. Uremic Toxins and Lipases in Haemodialysis: A Process of Repeated Metabolic Starvation. Toxins 2014, 6, 1505-1511.

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